Thomas C J, Rankin A J, Head G A, Woods R L
Baker Medical Research Institute, Prahran, Victoria, Australia.
Hypertension. 1997 May;29(5):1126-32. doi: 10.1161/01.hyp.29.5.1126.
Baroreflex control of heart rate in spontaneously hypertensive rats (SHR) is defective, largely because of a poor vagal contribution to the reflex. We have demonstrated previously that atrial natriuretic peptide (ANP) enhances reflex bradycardia in normotensive rats through an action on nonarterial vagal afferent pathways. In the present study, we investigated whether ANP could reverse the baroreflex abnormality in SHR. Heart rate reflexes were activated by three different methods in conscious, instrumented SHR and Wistar-Kyoto rats (WKY) in the presence of intravenous infusions of vehicle (saline) or rat ANP (150 ng/kg per minute). Heart rate responses were measured by (1) the steady-state changes in blood pressure after alternating slow infusions (over approximately 15 to 30 seconds) of a pressor (methoxamine) and depressor (nitroprusside) drug (stimulating predominantly arterial baroreceptors), (2) the ramp method of rapid infusion of methoxamine (over < 10 seconds; stimulating arterial and cardiopulmonary baroreceptors), and (3) the von Bezold-Jarisch method of activating chemically sensitive cardiac receptors through serotonin injections. ANP enhanced the heart rate range of the arterial baroreflex (steady-state method) by 13 +/- 3% in WKY but had no significant effect on the sensitivity or any other parameter of the steady-state baroreflex. When a very rapid rise in blood pressure was elicited by the ramp method in WKY, ANP significantly enhanced baroreflex bradycardia (sensitivity increased by 29 +/- 9%, P < .05). ANP also enhanced the bradycardia of the von Bezold-Jarisch reflex (by 33 +/- 16%, P < .05) in WKY. By contrast, ANP did not influence baroreceptor or chemoreceptor heart rate reflex responses in SHR. We conclude that in normotensive rats, ANP facilitates cardiopulmonary bradycardic reflexes. The lack of effect of ANP in SHR may be related to an underlying structural or genetic alteration in their cardiac sensors, perhaps associated with cardiac hypertrophy, that prevents the ANP-induced activation of cardiac sensory afferents, resulting in cardioinhibition.
自发性高血压大鼠（SHR）的压力反射对心率的控制存在缺陷，这主要是因为迷走神经对该反射的作用较弱。我们之前已经证明，心房利钠肽（ANP）通过作用于非动脉迷走神经传入通路增强正常血压大鼠的反射性心动过缓。在本研究中，我们调查了ANP是否能逆转SHR的压力反射异常。在清醒的、植入仪器的SHR和Wistar-Kyoto大鼠（WKY）中，静脉输注载体（生理盐水）或大鼠ANP（每分钟150 ng/kg），通过三种不同方法激活心率反射。通过以下方式测量心率反应：（1）交替缓慢输注升压药（甲氧明）和降压药（硝普钠）（主要刺激动脉压力感受器）后血压的稳态变化（约15至30秒）；（2）快速输注甲氧明的斜坡法（<10秒内；刺激动脉和心肺压力感受器）；（3）通过注射5-羟色胺激活化学敏感心脏感受器的冯·贝佐尔德-雅里什法。ANP使WKY的动脉压力反射心率范围（稳态法）增加了13±3%，但对稳态压力反射的敏感性或任何其他参数没有显著影响。当通过斜坡法在WKY中引起血压非常快速升高时，ANP显著增强压力反射性心动过缓（敏感性增加29±9%，P<.05）。ANP还增强了WKY中冯·贝佐尔德-雅里什反射的心动过缓（增加33±16%，P<.05）。相比之下，ANP对SHR的压力感受器或化学感受器心率反射反应没有影响。我们得出结论，在正常血压大鼠中，ANP促进心肺性心动过缓反射。ANP在SHR中缺乏作用可能与其心脏感受器潜在的结构或基因改变有关，可能与心脏肥大有关，这阻止了ANP诱导心脏感觉传入神经的激活，导致心脏抑制。
